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Patients having Glutathione S-transferase M1 allele and Apolipoprotein E E2 allele are predisposed to oxidative stress-induced cardiac injury.
The 6-TGN levels were not affected by the GSTM1 genotype.
Complex Haplotypes of GSTM1 Gene Deletions Harbor Signatures of a Selective Sweep in East Asian Populations.
These results illustrate the potential association between rs9642880 G > T and survival in hepatocellular carcinoma patients who received radiotherapy treatment.
GSTM1 and GSTT1 gene polymorphisms are not associated with lipid levels in endogenous hypertriglyceridemia in Chinese population.
This study suggests that GSTM1 active and GSTT1 null genotype combination might be a risk factor in developing mitochondrial disease.
The meta-analysis showed that glutathione S-transferases GSTT1 and GSTM1 null polymorphisms are risk factors for breast cancer [Meta-analysis].
individuals carrying GSTM1 null variant showed protective role against seizure.
Our meta-analysis supports that CYP1A1 exon7 polymorphism might contribute to individual susceptibility to esophageal cancer in the Chinese population. Gene-gene interaction analysis found a synergistic interaction between CYP1A1 mutation genotypes and GSTM1 deletion genotype.
The effects of GSTM1/GSTT1 genes on diabetes mellitus type 2 risk are gender dependent and may be triggered by tobacco smoking.
GSTM1 gene polymorphism is associated with liver diseases.
this is the first report on the GSTM1and GSTT1frequency distribution among the tribal population of western India.
Authors conclude that maternal GSTM1/GSTT1 gene polymorphisms present an impact on birth weight, being involved in the neonatal nutritional status.
VEGF, VEGFR2 and GSTM1 polymorphisms in outcome of multiple myeloma patients treated with thalidomide-based regimens
Based on our meta-analysis, the GSTM1 null genotype is a risk factor for CRC.
Indel variants of GSTM1 were typed in breast cancer patients and normal controls. GSTM1 deletion seemed to marginally increase breast cancer risk in Mexican women.
The current analyses suggests significant association was found between GSTM1 variants and the risk of childhood acute lymphoblastic leukemia (ALL), while no association were found between GSTT1 and GSTP1 Ile105Val polymorphism and childhood ALL risk
In conclusion, the present study indicated that GSTT1 deletion was associated with increased recurrence risk of breast cancer, while GSTM1 correlated with worst prognosis parameters at diagnosis, but was negatively associated with recurrence risk in luminal subtype samples.
Homozygous deletion of GSTM1 is associated with slower HIV disease progression.
The patients homozygous for the GSTM1 null alleles showed a 3.5 increased risk of Alzheimer's disease
missense mutation (rs135955605) associated with significant decrease of sperm motility and ATP content
Six proteins were regulated at both basal and inducible levels exhibiting the largest dynamic range of Nrf2 regulation: cytochrome CYP2A5, GSTM3, GSTM1, ENTPD5,UDPGDH, and EPHX1.
mitochondrial Gstb1 is induced under oxidative stress
the gene (GSTM1) encoding the detoxification enzyme glutathione S-transferase M1 is transcriptionally upregulated by Myb
The Gstm1 gene was represented by two EST clones with similar levels of downregulation.
We overexpressed Hoxa9 and Meis1 in primary hematopoietic cells. Arrays identified c-Myb and a c-Myb target (Gstm1) among the genes with the strongest response to Hoxa9/Meis1.
Genetic variants that cause a decremental change in expression of Gstm1 may permit an environment of exaggerated oxidative stress, leading to susceptibility to vascular remodeling and atherosclerosis
The role of polymorphisms of glutathione S-transferases GSTM1, M3, P1, T1 and A1 in susceptibility to alcoholic liver disease. In addition, oxidant stress is proposed to be an important pathogenic factor in liver damage related to alcohol.
Cytosolic and membrane-bound forms of glutathione S-transferase are encoded by two distinct supergene families. At present, eight distinct classes of the soluble cytoplasmic mammalian glutathione S-transferases have been identified: alpha, kappa, mu, omega, pi, sigma, theta and zeta. This gene encodes a glutathione S-transferase that belongs to the mu class. The mu class of enzymes functions in the detoxification of electrophilic compounds, including carcinogens, therapeutic drugs, environmental toxins and products of oxidative stress, by conjugation with glutathione. The genes encoding the mu class of enzymes are organized in a gene cluster on chromosome 1p13.3 and are known to be highly polymorphic. These genetic variations can change an individual's susceptibility to carcinogens and toxins as well as affect the toxicity and efficacy of certain drugs. Null mutations of this class mu gene have been linked with an increase in a number of cancers, likely due to an increased susceptibility to environmental toxins and carcinogens. Multiple protein isoforms are encoded by transcript variants of this gene.
GST HB subunit 4
, GST class-mu 1
, HB subunit 4
, S-(hydroxyalkyl)glutathione lyase
, glutathione S-alkyltransferase
, glutathione S-aralkyltransferase
, glutathione S-aryltransferase
, glutathione S-transferase M1
, glutathione S-transferase Mu 1
, GST 3-3
, GST Yb1
, glutathione S-transferase Yb-1 subunit
, glutathione-S-transferase mu type 1 (Yb1)
, glutathione-S-transferase, mu type 1 (Yb1)
, GST 1-1
, glutathione S-transferase GT8.7
, glutathione-S-transferase, mu 1
, glutathione S-transferase mu 1
, glutathione S-transferase mu 2
, glutathione S-transferase, mu 2